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The SMYD3-MEK/ERK Axis Contributes to Intestinal Metaplasia and H. pylori-associated Gastric Carcinogenesis

delete2026-05-20
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PRE
AI
Y
Yuka Hirashita *
Y
Yoshiyuki Tsukamoto
M
Masaaki Kodama
T
Takuro Uchida
S
Sotaro Ozaka
M
Masahide Fukuda
S
Shohei Terashi
H
Haruna Noguchi
K
Kei Mori
D
Daisuke Minezaki
K
Koshiro Tsutsumi
R
Ryota Sagami
K
Kensuke Fukuda
R
Ryo Ogawa
M
Mizuki Endo
S
Shusaku Kurogi
C
Chisato Nakada
N
Naoki Hijiya
H
Hidefumi Shiroshita
K
Kazunari Murakami
DOI：10.1016/j.labinv.2026.106137delete
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Abstract

Abstract

En 中文
Chronic Helicobacter pylori (H. pylori) infection induces gastric atrophy and intestinal metaplasia (IM), which are key precancerous lesions for gastric cancer (GC). The purpose of this study was to determine the mechanisms by which MEK/ERK signaling persists from active infection through the post-eradication stage and contributes to gastric carcinogenic risk.
Keywords:
SMYD3
MEK/ERK signaling
Helicobacter pylori
intestinal metaplasia
gastric carcinogenesis

Journal

Laboratory Investigation cover
Laboratory Investigation
IF:
4.2
Papers:
5.4K
Citations:
1.1W

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